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The hexosamine signaling pathway: O-GlcNAc cycling in feast or famine. | LitMetric

The hexosamine signaling pathway: O-GlcNAc cycling in feast or famine.

Biochim Biophys Acta

Laboratory of Cell Biochemistry and Biology, NIDDK, National Institutes of Health, Bethesda, MD 20892, USA.

Published: February 2010

AI Article Synopsis

  • The hexosamine signaling pathway (HSP) connects nutrient availability to the O-GlcNAc modification of key proteins, influencing various cellular processes.
  • Enzymes involved in O-GlcNAc cycling work alongside traditional signaling pathways to regulate growth and metabolism by acting as a binary switch between anabolic and catabolic functions.
  • This review highlights the significant role of O-GlcNAcylation in cellular signaling and its potential links to diseases such as diabetes, cancer, and neurodegenerative disorders.

Article Abstract

The enzymes of O-GlcNAc cycling couple the nutrient-dependent synthesis of UDP-GlcNAc to O-GlcNAc modification of Ser/Thr residues of key nuclear and cytoplasmic targets. This series of reactions culminating in O-GlcNAcylation of targets has been termed the hexosamine signaling pathway (HSP). The evolutionarily ancient enzymes of O-GlcNAc cycling have co-evolved with other signaling effecter molecules; they are recruited to their targets by many of the same mechanisms used to organize canonic kinase-dependent signaling pathways. This co-recruitment of the enzymes of O-GlcNAc cycling drives a binary switch impacting pathways of anabolism and growth (nutrient uptake) and catabolic pathways (nutrient sparing and salvage). The hexosamine signaling pathway (HSP) has thus emerged as a versatile cellular regulator modulating numerous cellular signaling cascades influencing growth, metabolism, cellular stress, circadian rhythm, and host-pathogen interactions. In mammals, the nutrient-sensing HSP has been harnessed to regulate such cell-specific functions as neutrophil migration, and activation of B-cells and T-cells. This review summarizes the diverse approaches being used to examine O-GlcNAc cycling. It will emphasize the impact O-GlcNAcylation has upon signaling pathways that may be become deregulated in diseases of the immune system, diabetes mellitus, cancer, cardiovascular disease, and neurodegenerative diseases.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2815088PMC
http://dx.doi.org/10.1016/j.bbagen.2009.07.017DOI Listing

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